We shall investigate the mechanism by which a reduced carboxamidomethylated curarimetic neurotoxin of cobra venom origin protects guinea pigs against the development of experimental allergic encephalomyelitis (EAD), an animal model disease for human multiple sclerosis. Enzymatic cleavage of derivatized neurotoxin and chemical synthesis of specific toxin peptide fragments and analogs will be performed. These peptides will be used to test the idea that specific portions of the molecule control its immunosuppressive behavior. Immune cells derived from toxin or peptide protected animals will be transferred to histocompatible recipients; challenge with myelin basic protein will not induce EAE if unresponsiveness has been transferred. The properties of the cell subpopulation(s) involved in effecting the unresponsive state will be determined.